The currently active human mobile elements families (L1, Alu, and SVA) are well established as significant contributors to genetic instability and associated genetic diseases, including cancer. Current estimates attribute 0.5% of human inherited genetic disorders as having been the consequence of mobile element insertions and/or subsequent mutagenic recombinations. While most mutagenesis studies concerning mobile elements tend to focus on disruptive insertion events, recombinations between non-allelic mobile elements can result in genetic loss, duplication, and/or rearrangements, all of which contribute to the overall somatic mutation burden. The frequencies at which these mutagenic events occur in somatic tissues, as well as the factors that modulate that frequency, remain largely unexamined. Although the number of de novo mobile element insertions occurring in somatic cells is generally considered to be quite low, recent evidence indicates that L1 elements produce orders of magnitude more double-stranded breaks (DSBs) than de novo insertions. As double-stranded breaks are known to instigate non-allelic recombination, these new data offer us compelling reason to investigate mutagenic recombination between interspersed repeats and the ability of L1 endonuclease to instigate these events. [unreadable] [unreadable] [unreadable]